Salmonella typhi survives within macrophages after phagocytosis. The virulence gene regulatory system that upregulates genes needed for intracellular survival within phagolysosomes is:
- A Salmonella Pathogenicity Island 2 (SPI-2) encoded T3SS that modifies the Salmonella-containing vacuole ✓
- B SPI-1 encoded T3SS that translocates effectors triggering membrane ruffling for invasion
- C Vi antigen (capsular polysaccharide) blocking complement activation
- D OmpC/OmpF porins that sense acidic pH in lysosomes
Explanation
After initial invasion via SPI-1 T3SS, intracellular Salmonella within the Salmonella-containing vacuole (SCV) activates SPI-2 encoded T3SS which translocates effectors (SseF, SseG, SifA) that modify vacuolar membrane composition, prevent lysosome fusion and phagosome acidification, and establish the SCV as a replication niche. SPI-1 functions at the invasion stage to inject effectors causing actin rearrangement and bacterial uptake. Vi antigen reduces opsonization but is relevant extracellularly. OmpC/OmpF are outer membrane porins regulating permeability.
Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.
High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP
Written and medically reviewed by the StethoPrep medical team.